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miR-34a is a microRNA safeguard for Citrobacter-induced inflammatory colon oncogenesis

Lihua Wang1,2,3,4, Ergang Wang3,4, Yi Wang3,4,5

  • 1Key Laboratory of RNA Biology, Key Laboratory of Protein and Peptide Pharmaceutical, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.

Elife
|December 14, 2018
PubMed

Insights

MicroRNA miR-34a protects the colon stem cell niche during inflammation. Its deficiency promotes colon tumorigenesis by allowing uncontrolled stem cell proliferation and immune cell infiltration.

Area of Science:

  • Molecular Biology
  • Immunology
  • Gastroenterology

Background:

  • Inflammation drives tissue repair but chronic inflammation can lead to tumorigenesis.
  • Stem cell niches are critical for tissue regeneration and are vulnerable during inflammation.

Purpose of the Study:

  • To investigate the role of microRNA miR-34a in protecting the stem cell niche during inflammation.
  • To understand how miR-34a deficiency contributes to colon tumorigenesis.

Main Methods:

  • Investigated miR-34a function in a mouse model of colon inflammation and tumorigenesis.
  • Utilized genetic deficiency models for miR-34a.
  • Analyzed immune cell populations and stem cell proliferation in the colon.

Main Results:

  • miR-34a deficiency led to colon tumorigenesis following Citrobacter rodentium infection.
  • miR-34a restrains inflammation-induced stem cell proliferation by targeting immune and epithelial cells.
  • miR-34a targets IL-6R, IL-23R, CCL22, and IL-17RD to regulate T helper 17 cell responses and stem cell proliferation.

Conclusions:

  • miR-34a is crucial for safeguarding the stem cell niche and promoting reparative regeneration during inflammation.
  • Dysregulation of miR-34a contributes to inflammation-driven colon cancer development.
Keywords:
Citrobacter rodentiumTh17cancer biologycolon cancerinflammationmousestem cell

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